Dr. Ballinger received his BS and MS degrees from Texas A&M University and his PhD degree in biochemistry from Emory University. He completed postdoctoral training at the University of Vermont's Genetics and Toxicology Laboratory, initially as an environmental pathology fellow and later as a Department of Energy Alexander Hollaender Distinguished Fellow.

There is growing evidence that many forms of disease can be initiated by free radical mediated events or energetic deficits that can be related to cellular stress and damage. A cellular source and target of free radical production and damage is the mitochondrion. Because mitochondria are essential for multiple cell functions, including energy production, cell signaling, cell growth, proliferation, and programmed cell death, we hypothesize that free radicals cause mitochondrial damage and dysfunction in cells important in various disease processes, and furthermore, that disease risk factors increase mitochondrial damage and dysfunction. Specifically, we hypothesize that fetal and/or childhood exposure to cardiovascular disease risk factors increases the risk of adult disease development by causing mitochondrial damage and dysfunction. Finally, we also hypothesize that the mitochondrion plays a major role in influencing individual disease susceptibility by mitochondrial – nuclear interaction processes, and that environmentally influenced selection events for mitochondrial function that conveyed increased reproductive and survival success during the global establishment of human populations during prehistoric times, today, influence human disease susceptibility.